Endocrinology Flashcards
Endocrine portion of pancreas
Islet of Langerhans (mostly full of B cells that secrete insulin)
Normal physiology of glucose
High glucose stimulate insulin release from B cells
Pathophysiology of DM1
Destruction of pancreatic B cells (mostly autoimmune and rest are idiopathic) leads to decreased insulin secretion and hyperglycemia
2 peaks of type 1 DM
Mid childhood (age 4-6) and early puberty (10-14)
Incidence of DM in the world
Colder population and further from the equator has an increased incidence
Non-modifiable risk factors of type 1 DM
White population is highest
Possible environmental risk factors of type 1 DM
Viral infections (EBV, Coxsackier, CMV)
Diet
Higher socioeconomic status
Obesity
Diet risk factors for type 1 DM
Increased risk with exposure to cows milk and early cereal introduction
Decreased risk with breastfeeding and solid food at later ages
3 presentations of type 1 DM
Classic (3 Ps and weight loss/fatigue)
DKA (fruit smelling, drowsy)-hospitalize, hydrate, insulin
Silent (incidental) discovery
Diagnostic criteria of type 1 DM
Fasting plasma glucose >126
Random plasma glucose >200 mg/dL
(Plasma glucose >200 2 hrs after oral glucose tolerance test
HbA1C >6.5)
What to do when kid presents with type 1 for first time or DKA?
Hospitalize
Common sxs of hypoglycemia
Irritability, shaking, dizziness, sweating, nausea
Goals of type 1 tx
Achieve glucose control without hypoglycemia (higher risk when 4,5 and 6)–decreased risk when get older
Set goals
Target for ideal fasting blood glucose and HbA1C based on age
<5: 80-200 and 7.5-8.5%
6-11: 70-180 and <8%
12-19: 70-150 and <7.5%
Types of insulin
Rapid acting (lispro, aspart) Short acting (regular insulin)- pre meal bolus 5-30 min before meal Intermediate acting (NPH insulin)-combo with long Long-acting (glargine, detemir) administer 1-2x/day
Which insulins are used to combat a significant increase in blood glucose?
Rapid and short acting
Physiologic regimen for insulin dosing
Basal: intermediate or long acting to suppress hepatic glucose production
Bolus: rapid or short acting to cover carb intake at meals
1 unit per kilo over 24 hrs (half and half)
Definition of obesity
Normal is 5th-85th percentile
Overweight is 85-95th percentile
Obese is >95th percentile
Severe obesity is >120th
When is obesity more common ethnically?
American Indian, black and Mexican Americans
What is a strong predictor of adult obesity?
Childhood obesity
General nutrition recommendations
Stabilize weight or small weight loss is obese Portion control Avoid sugary drinks Limit milk intake (after 1) 900-1200 kcal/day when 6-12 Eat at home
Exercise recommendations
30-60 min of activity per day
Non-academic screen time to 2 hrs per day
Risk factors of type 2 DM
Obesity
Family hx
Native American, African American, Latino, Asian American or Pacific Islander
Conditions associated with insulin resistance
Sxs of type 2
Polydipsia and polyuria Visual disturbances Infections Most are asymptomatic Fatigue, irritable, can't concentrate
Acanthosis nigricans
Risk factor for type 2 (excess keratin makes skin thicker due to receptors for insulin)
When do you screen for type 2 DM in kids?
Screen kids >10 YO if overweight/obese AND have 2 or more of following:
type 2 DM in first or second degree
high risk ethnic group
signs of insulin resistance
maternal hx of DM or gestational diabetes when kid in utero
*every 3 yrs
Tx for type 2 overview
Lifestyle Treat psychosocial aspects Metformin and insulin Prevent macro and microvascular complications Comorbidities
First line tx type 2
Metformin
When is insulin recommended along with metformin and lifestyle changes?
Random plasma glucose >250 or HbA1C>9%
Monitoring for type 2
Review weight, DMI, diet and activity
Blood glucose monitoring 3/day on insulin
Monitor A1c every 3 mos
Lab tests for HTN and hyperlipidemia
First line tx for HTN with type 2 DM
ACE-i or ARBs
second is thiazides, CCBs or BBs
Why do we not like BB for DM?
Masks sxs of hypoglycemia
Stages of HTN
Stage 1 is 130/80-139/89
Stage 2 is >140/90
Goals for lipid levels in adolescents in DM
LDL<100
HDL>35
TAGs<150
Tx recommendation for hyperlipidemia
6 mos no meds first and then HMG CoA reductase inhibitors if LDL>130 if over 10 and obese
What is short stature?
Height 2 standard deviations below mean (<2.3 percentile)
Most widely used system to measure skeletal age
Greulich-Pyle Atlas method
Normal variants of growth leading to short stature
Familial short stature
Constitutional delay of growth (most common)
Idiopathic short stature
Small for age
Pathologic Causes of growth failure
Systemic disease Endocrine (Cushings, hypothyroidism, GH deficiency, sexual precocity) Genetic syndromes (turner, PWS, noonans, achondroplasia)
What is familial short stature?
Kid is small b/c parents are short
Bone age is normal
How to check mean parental height to consider familial short stature
Girls: 5 in taken off fathers height and avg with mom
Boys: 5 in added to mom and avg with dad
What is constitutional delay of growth?
Later bloomers b/c late growth spurt
Bone is delayed and corresponds with height
Usually parents were delayed too
How to diagnose GH deficiency
R/o hypothyroidism, turners and skeletal disorders
If none of them then do IGF-1, IGFBP-3, bone age (and maybe GH stimulation test)
First line treatment for GH deficiency
Recombinant human growth hormone therapy (must be before growth plate closes)
Daily SC injections
Side effects of rhGH
Psuedotumor cerebri
Hyperglycemia or insulin resistance
Gynecomastia
Increase T4 conversion without hypothyroidism
What is Noonan syndrome?
Autosomal dominant
Short stature
CHD (pulmonic stenosis)
Variable genetic mutations
Most common cause of pathologic obesity and short stature
PWS (chromosome 15)
What is achondroplasia?
Autosomal dominant caused by mutations in FGFR3 gene (fibroblast growth factor)
Features of achondroplasia
Disproportionate short stature with rhizomelic shortening-proximal bones shortened like humerus and femur
Macrocephaly
Normal cognition
Brachydactylyl and single transverse palmar crease
Gigantism
GH excess prior to closure of epiphyses so excessive growth of long bones (rare compared to acromegaly)
Diagnostics for GH excess
Increased serum IGF-1
GH suppression test (administer glucose and if GH fails to fall below 1 ng/mL then abnormal)
MRI to look at pituitary and hypo
Tx for GH excess
Surgery, radiation,
Octreotide, bromocriptine
Normal age of puberty
Boys 9-14 YO
Girls 8-14 YO
Definition of precocious puberty
Onset of secondary sex characteristics before 8 in girls and before 9 in boys
Central precocious puberty
Gonadotropin dependent to elevated GnRH and gonadotropins
Short stature
Peripheral precocious puberty
Gonadotropin independent so elevated gonadal steroids with low gonadotropins
Causes of central precocious puberty
Idiopathic mostly or CNS tumors or abnormalities
Girls
Studies for central precocious puberty
LH and FSH high
Also do estradiol and testosterone
Tx of central precocious puberty
GnRH analogue
Causes of peripheral precocious puberty
Exposure to gonadal steroids outside of HPG axis
Congenital adrenal hyperplasia
McCune albright Syndrome (females)
*normal LH, FSH levels
What is pubertal gynecomastic?
Benign
Causes of prepubertal gynecomastia
Klinefelters
Aromatization due to obesity
Adrenal or testicular neoplasm
Most common cause of contra sexual development
Congenital adrenal hyperplasia
Most common reason for congenital adrenal hyperplasia
21 hydroxylase deficiency
